BAIT
BRD2
D6S113E, FSH, FSRG1, NAT, RING3, RNF3, DADB-17J1.3
bromodomain containing 2
GO Process (3)
GO Function (3)
GO Component (0)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Homo sapiens
PREY
FGFR3
ACH, CD333, CEK2, HSFGFR3EX, JTK4
fibroblast growth factor receptor 3
GO Process (27)
GO Function (4)
GO Component (3)
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- JAK-STAT cascade [TAS]
- bone maturation [ISS]
- bone mineralization [ISS]
- bone morphogenesis [ISS, TAS]
- chondrocyte differentiation [TAS]
- chondrocyte proliferation [TAS]
- endochondral bone growth [TAS]
- endochondral ossification [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor apoptotic signaling pathway [IMP]
- fibroblast growth factor receptor signaling pathway [IDA, IGI, TAS]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- negative regulation of developmental growth [ISS]
- neurotrophin TRK receptor signaling pathway [TAS]
- peptidyl-tyrosine phosphorylation [IDA]
- phosphatidylinositol-mediated signaling [TAS]
- positive regulation of ERK1 and ERK2 cascade [IMP]
- positive regulation of MAPK cascade [IMP]
- positive regulation of cell proliferation [IGI, IMP]
- positive regulation of phosphatidylinositol 3-kinase activity [IMP, TAS]
- positive regulation of phospholipase activity [IMP]
- positive regulation of tyrosine phosphorylation of Stat1 protein [IMP]
- positive regulation of tyrosine phosphorylation of Stat3 protein [IMP]
- protein autophosphorylation [IDA]
- skeletal system development [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Negative Genetic
Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.
Publication
Synergistic drug combinations for cancer identified in a CRISPR screen for pairwise genetic interactions.
Identification of effective combination therapies is critical to address the emergence of drug-resistant cancers, but direct screening of all possible drug combinations is infeasible. Here we introduce a CRISPR-based double knockout (CDKO) system that improves the efficiency of combinatorial genetic screening using an effective strategy for cloning and sequencing paired single guide RNA (sgRNA) libraries and a robust statistical scoring ... [more]
Nat. Biotechnol. Mar. 20, 2017; 0(); [Pubmed: 28319085]
Quantitative Score
- -3.103 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- CRISPR GI screen
- Cell Line:K562 (EFO:0002067)
- Experimental Setup:Timecourse
- GIST: A-phenotypic negative genetic interaction
- Library:Drug Target-CDKO CRISPRn library
- Significance Threshold: q-value<0.05
Curated By
- BioGRID